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अमूर्त

The Ammonia Hypothesis of Hepatic Encephalopathy should be Revisited

Matthew McMillin and Sharon DeMorrow

Hepatic Encephalopathy (HE) is a neurological complication of the brain following liver damage that was classically thought of being a functional decline in neuronal activity due to metabolic disturbances. Acute liver failure as well as chronic liver diseases can cause HE, with the progression of HE correlating to the severity of liver damage. Initially there are disturbances in cognition, that then progress to disruptions in motor control, and finally global suppression of neural circuits, which can lead to coma. The first factor identified as a causal link and a treatment point for HE was ammonia. However, recent research has begun to elucidate strong support for other pathological processes in this disorder as well. Due to these varying ideas on the progression of HE, this editorial will discuss why the ammonia hypothesis of HE pathogenesis is supported by current research as well as some strong counterpoints that refute this hypothesis.

Ammonia does play a part in HE pathogenesis, the studies conducted clinically and using animal models have demonstrated that other elements must be involved with HE progression to explain pathogenesis not accounted for by ammonia toxicity. As it stands, ammonia seems to play a significant role in chronic liver disease states while playing a small role during acute liver failure and minimal hepatic encephalopathy. Future studies will need to find ways to isolate these pathological processes in various acute and chronic liver damage models to fully identify the pathological effects of ammonia. In conclusion, ammonia does play a role in HE progression but due to its lack of involvement in some aspects of HE progression, there is the need to investigate its interplay with other pathological processes to help develop better therapeutic treatments options for HE.